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Biomedical subjects

C D Cohen

Publications and source records attributed to C D Cohen.

13 recordsLinked to original sources
PubMed2002

[Gene expression profiling in prostatic cancer].

Basic aspects of the biology and molecular alterations in prostate carcinoma remain poorly understood. New diagnostic and prognostic markers for prostate carcinoma may add additional information to current histopathological diagnosis. In order to achieve these goals, a comprehensive gene expression analysis was performed on non-metastasizing, untreated prostate cancer tissues. RNA expression profiles of approximately 12,600 sequences from 26 human prostate tissues (17 adenocarcinomas and 9 normal adjacent to cancer tissues) were investigated using high-density oligonucleotide microarray technology (Affymetrix). We identified 63 genes which were significantly increased (at least 2.5-fold) and 153 genes which were decreased (at least 2.5-fold). Upregulated genes included several which had not yet been described, such as the genes encoding the specific granule protein (SGP28), several members of the histone family, and the alpha-methylacyl-CoA racemase, but also previously reported ones such as hepsin, LIM domain kinase 2, and carcinoma-associated antigen GA733-2. Laser capture-microdissection of epithelial and stromal compartments from cancer and histologically normal specimens followed by an amplification protocol for low amounts of RNA (< 0.1 microgram) allowed us to distinguish between gene expression profiles characteristic of epithelial cells and those typical of stroma. Most of the genes identified in bulk tumor material as upregulated were indeed overexpressed in cancerous epithelium rather than in the stromal compartment. DNA microarray data for up- and downregulated genes were confirmed by quantitative RT-PCR. We demonstrated that development of prostate cancer is associated with downregulation as well as upregulation of genes that show complex differential regulation in epithelia and stroma. Some of the alterations in gene expression identified in this study may prove useful in development of novel diagnostic and therapeutic strategies. Gene expression profiling of microdissected tumor cells in prostate biopsies may supplement histopathologic diagnosis.

Adenocarcinoma↗
PubMed2001

Hyponatraemia as a complication of colonoscopy.

A case of colonoscopy-induced hyponatraemic encephalopathy led us to study the risk of hyponatraemia after gastrointestinal endoscopy. We assessed 40 patients before and after colonoscopy. 20 gastroscopy patients served as controls. Our findings show a high incidence (7.5%) of hyponatraemia after colonoscopy, in association with raised serum concentrations of arginine vasopressin. Physicians should be aware of this complication, since it may contribute to psychological and neurological symptoms after colonoscopy.

Arginine Vasopressin↗
PubMed2001

Chemokine-Induced secretion of gelatinase B in primary human monocytes.

Chemokines help control normal leukocyte trafficking as well as their infiltration into tissues during acute and chronic inflammation. Matrix metalloproteinases (MMPs) help support the extravasation and infiltration of leukocytes through limited proteolysis of basement membranes and matrix material. The effect of the chemokines RANTES/CCL5, MCP-1/CCL and SDF-1/CXCL12 on secretion of the matrix metalloproteinase B and its endogenous inhibitor TIMP-1 was studied. RANTES/CCL5 and SDF-1/CXCL12 were found to induce MMP-9 secretion in primary human monocytes while TIMP-1 secretion was not affected. RANTES/CCL5 effects were mediated through CCR1 because the CCR1 antagonist BX471 was found to effectively block RANTES/CCL5-induced MMP-9 secretion.

Chemokines↗
PubMed1996

K+ currents of human T-lymphocytes are unaffected by Alzheimer's disease and amyloid beta protein.

Alterations of Ca2+ homeostasis have been reported for both fibroblasts and T-lymphocytes of patients with Alzheimer's disease (AD). Considering the importance of K+ conductances for the cellular Ca2+ regulation and the recently reported absence of a K+ channel in Alzheimer fibroblasts, we investigated K+ currents in T-lymphocytes of patients with AD. In addition, the finding that amyloid beta protein affects the Ca2+ signal of T-lymphocytes and the function of K+ channels in fibroblasts prompted us to study a possible influence of amyloid beta protein fragments on K+ channels of T-lymphocytes. Our data, obtained by means of the whole-cell patch-clamp configuration on freshly isolated T-lymphocytes, indicate that K+ channels of these cells do not present any functional deficit in AD, and amyloid beta protein does not mediate an alteration of their currents.

Alzheimer Disease↗
PubMed1984

Phaeochromocytoma and acute cardiovascular death (with special reference to myocardial infarction).

The causes of death, as determined by autopsy, in 10 patients dying from the acute effects of phaeochromocytoma were myocardial infarction (five patients), left ventricular failure (two patients), cerebral haemorrhage (two patients) and circulatory collapse with malignant phaeochromocytoma (one patient). Most patients died shortly after admission during the course of a fulminant cardiovascular illness and the underlying tumour was unsuspected in eight instances. The clinical features and post-mortem cardiovascular findings are reviewed.

Adrenal Gland Neoplasms↗
PubMed1983

Hepatic complications of antituberculosis therapy revisited.

Since 1973, when the incidence and pattern of adverse reactions to antituberculosis therapy were described by Rossouw and Saunders, para-amino-salicylic acid, the major cause of drug-induced hepatitis, has been withdrawn from the regimen used in Cape Town and replaced with pyrazinamide (PZA). Our study in the same hospital indicates that although the substitution has resulted in a significant reduction in the incidence of all side-effects (4,1% v. 9%; P less than 0,001), the incidence of hepatitis is unchanged (0,3%). PZA is currently the major cause of hepatitis associated with antituberculosis therapy.

Adolescent↗
PubMed1981

Hepatic sequelae of congestive cardiac failure. Evidence for a liver lesion in patients in whom cardiac function has been restored to normal.

In order to test the hypothesis that clinical and biochemical features of liver disease due to cardiac failure regress upon relief of cardiac decompensation, 38 patients with constrictive pericarditis were studied before and after pericardiectomy for periods ranging from 1 week to 25 years. All patients were judged to be free of clinical evidence of heart failure. Hepatomegaly was present in 10 of the 38 patients studied. Of the patients studied 1-25 years after operation, 96% had elevated serum levels of total and conjugated bilirubin. The percentage Bromsulphalein (BSP) retention at 45 minutes was abnormal in all 29 patients studied 1 year or more after surgery. There was no significant correlation between the level of bilirubin or the percentage BSP retained when these were compared with the pre-operative height of jugular venous pressure, degree of pulsus paradoxus, duration of symptoms or degree of hepatic congestion. Our study reveals that the liver lesion of cardiac failure persists for up to 25 years after restoration of normal cardiac function.

Adolescent↗
PubMed1980

Takayasu's syndrome--evidence for a liver lesion.

Liver function tests were carried out in 40 patients with Takayasu's syndrome. The alkaline phosphatase level was elevated in 73% of patients, the SGOT level in 59%, and the lactic dehydrogenase level in 84,6%. In contrast, creatinine phosphokinase levels were elevated in only 23.5% and bilirubin levels were normal in all patients. Histological abnormalities were present in 3 out of 5 patients in whom a biopsy had been performed. These abnormalities may shed light on the aetiology of this syndrome.

Adolescent↗
PubMedDate not supplied

Altering glomerular epithelial function in vitro using transient and stable transfection.

Damage of the glomerular filtration barrier leads to proteinuria and progressive renal failure. Several independent lines of research have implicated the glomerular epithelial cell (GEC) as a key player in initiation and propagation of pathways leading to glomerulosclerosis. A growing number of molecules activated in this process have been identified. To further define their cellular function, manipulation of these molecules using pharmacological or genetic approaches in tissue culture systems are required. In this study, strategies for altering GEC gene expression by transient and stable transfection of fluorescence labeled proteins will be presented and discussed. The insight gained through these and comparable systems should allow a detailed dissection of the molecular pathways active in GEC function and failure.

Cells, Cultured↗